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Coupling the modules of EMT and stemness: A tunable 'stemness window' model.

Mohit Kumar Jolly1,2, Dongya Jia1,3, Marcelo Boareto1,4

  • 1Center for Theoretical Biological Physics, Rice University, Houston, TX 77005-1827, USA.

Oncotarget
|August 29, 2015
PubMed
Summary

Cancer cell migration and tumor initiation are linked to Epithelial-to-Mesenchymal Transition (EMT) and stemness. This study reveals how OVOL fine-tunes this interplay, suggesting partial EMT phenotypes are key for stemness.

Keywords:
OVOLcancer stem cellsmultistabilitypartial EMTstemness window

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Area of Science:

  • Cell Biology
  • Cancer Research
  • Theoretical Biology

Background:

  • Carcinoma metastasis involves tumor cell migration and secondary tumor formation.
  • Epithelial-to-Mesenchymal Transition (EMT) and cellular stemness are crucial for metastasis.
  • The relationship between EMT states (complete vs. partial) and stemness remains unclear.

Purpose of the Study:

  • To theoretically investigate the correlation between EMT and stemness.
  • To explore how factors like OVOL modulate the EMT-stemness interplay.
  • To reconcile conflicting experimental findings on EMT and stemness.

Main Methods:

  • Developed a theoretical framework coupling core EMT (miR-200/ZEB) and stemness (LIN28/let-7) modules.
  • Modeled the influence of OVOL on the EMT-stemness regulatory circuit.
  • Analyzed the 'stemness window' positioning along the 'EMT axis'.

Main Results:

  • Demonstrated that the 'stemness window' on the 'EMT axis' is not fixed and can be modulated.
  • Showed that OVOL, coupled with the miR-200/ZEB/LIN28/let-7 circuit, fine-tunes EMT-stemness.
  • OVOL inhibits stemness in fully mesenchymal cells while enhancing it in hybrid EMT (E/M) cells.

Conclusions:

  • The study unifies contradictory findings on EMT and stemness.
  • Supports the emerging concept that partial EMT phenotypes are associated with stemness.
  • Provides new, testable predictions for cancer research.